期刊
INFLAMMATION RESEARCH
卷 60, 期 1, 页码 47-53出版社
SPRINGER BASEL AG
DOI: 10.1007/s00011-010-0233-1
关键词
Chronic hepatitis B; PD-1/PD-L; Intrahepatic protein expression; Inflammation
资金
- National Natural Science Foundation of China [30771905]
- National Basic Research Program of China (973 Program) [2007CB512800]
- Mega-projects of Science Research [008ZX10002-008]
- Beijing Municipal Science & Technology Commission [D08050700650803]
Background and objective Programed cell death-1 (PD-1) represents a mechanism of T-cell dysfunction in hepatitis B virus (HBV) persistence. In peripheral blood, PD-1 is up-regulated in virus-specific T cells, leading to the impairment of T cells. This study investigated the intrahepatic expression of PD-1 and its ligand (PD-L) in patients with chronic hepatitis B (CHB) virus. Methods Liver specimens were obtained from CHB (n = 56), acute hepatitis B (AHB, n = 12) patients and age-matched healthy subjects (n = 10). The expression of PD-1/PD-L was determined by immunohistochemistry. Results In CHB patients, PD-1 was predominantly expressed in lymphocytes infiltrating the portal tract. PD-L1 was detected in lymphocytes, hepatocytes and liver sinusoidal endothelial cells, while PD-L2 was localized in Kupffer cells and dendritic cells. The labeling indexes of PD-1 and PD-L I in lymphocytes infiltrating portal area were significantly higher in CHB patients than in healthy controls and AHB patients. Within the CHB patients, the increases in labeling indexes of PD-1 and PD-L paralleled the degree of inflammation. Conclusions These results suggest that over-expression of PD-1, PD-L1 and PD-L2 within liver may participate in local immune dysfunction, which could be one of the mechanisms involved in the chronicity of HBV infection and chronic inflammation seen in CHB patients.
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